Blood

Barrier failure changes two clinical variables at once: fluid movement into brain tissue and access of substances to the central nervous system. The neurovascular unit normally keeps plasma proteins, cells, and most drugs in the circulation. When inflammatory, ischemic, traumatic, or hypertensive injury loosens that seal, protein-rich fluid enters the extracellular space and may raise intracranial pressure. The same opening can increase exposure of neural tissue to drugs or toxins; as the barrier recovers, CSF penetration of an antimicrobial can fall again. The first bedside distinction is vasogenic versus cytotoxic edema. Vasogenic edema reflects leakage through a disrupted barrier. Cytotoxic edema reflects swollen cells, initially with the barrier relatively intact. Ischemia can produce both in sequence, so a patient may move from cellular injury to barrier leak and reperfusion-related hemorrhage. This distinction prevents a common treatment error: dexamethasone can reduce tumour-associated vasogenic edema but is not a treatment for ischemic-stroke or intracerebral-haemorrhage edema. A new decline in consciousness, seizure, severe headache, visual change, focal deficit, or pupil asymmetry is not simply a label of BBB disruption. It is a signal...